The objective of this study is to investigate the role of the systemic arterial circulation in the pulmonary vascualar response to atelectasis or hypoxia in the conscious, spontaneously breathing dog. We have demonstrated that the reduction in blood flow to an acutely hypoxic lung depends upon systemic PO2 in conscious, spontaneously breathing dogs. If systemic arterial PO2 is kept at or above normal levels, then blood flow to the hypoxic lung decreased. However, if PaO2 is allowed to fall or if the arterial chemoreceptors are stimulated with NaCN, then the reduction of blood flow to the affected areas is much less pronounced. This is not seen in sinoaortic denervated dogs. After a control period of bilaterial 100% O2, dogs with electromagnetic flow probes chronically implanted on the left and main pulmonary artery and breathing through Carlens dual-lumen endotracheal tubes will either be subjected to left lung atelectasis or 100% N2 ventilation of the left lung. Redistribution of pulmonary blood flow away from the unilaterally hypoxic or atelectatic lung will be assessed by the change in the ratio of left pulmonary artery blood flow to main pulmonary artery blood flow. Systemic reflexes will be stimulated by administering room air to the "normoxic" lung to lower PaO2 or NaCN injection (chemoreflex), or removal of moderate amounts of blood (baroreflex). Experiments will be repeated after adrenergic blockade, with constant or elevated PaCO2, and after sinoaortic denervation. The data obtained should contribute to our understanding of the control of pulmonary artery blood flow and ventilation-perfusion relationships and may be of great value in interpreting the "shock lung syndrome."